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554 Part VI: The Erythrocyte Chapter 37: Anemia of Chronic Disease 555

TABLE 37–3. Treatments of Anemia of Inflammation and Anemia of Chronic Kidney Disease
Modality Indications Typical Setting Risks and Side Effects Specific Benefits
Transfusion • Cardiac ischemia • Hgb <10 g/dL • Infections • Rapid correction of
• Lack of response to • Chest pain and electro- • Volume overload anemia
other modalities cardiogram changes • Transfusion reaction

Erythropoietin • Fatigue, exertional • Hgb <10 g/dL • Response takes several • Usually well tolerated,
intolerance • Anemia symptoms weeks relatively safe
• Balance against • Rare red cell aplasia
side effects in Hgb with some forms of
10–12 g/dL erythropoietin 107
• May worsen outcome in
some cancers 108
• Increased thromboembolic
events 79–82,96,109
• Expensive
Iron (oral or • Coexisting iron • Suspected or docu- • Gastrointestinal side effects • Inexpensive, relatively
parenteral) 51 deficiency mented iron deficiency (oral) safe
• Resistance to erythro- • Systemic and local reactions
poietin (investigational) (parenteral)
• May decrease resistance to
infections? 83,103–105

myeloid cells. Direct marrow examination is necessary to establish evidence to date has not resulted in a consensus on specific indications
the diagnosis. for intravenous iron or its optimal dosing. 83
5. Thalassemia minor is a common cause of mild anemia in many parts
of the world. It can be confused with AI (Chap. 48). Microcytosis THERAPY FOR ANEMIA OF INFLAMMATION
is a life-long condition and usually is more severe in this group of
disorders than in AI. EPO therapy for the treatment of AI has been tested in the setting of
6. Dilutional anemia is seen in pregnancy and in patients with severely various cancers, 84,85 multiple myeloma and other hematologic malignan-
increased plasma protein levels as a result of multiple myeloma or cies, 21,86,87 rheumatoid arthritis, 88–91 and inflammatory bowel diseases. 92,93
macroglobulinemia (Chap. 109). In most reports, more than 50 percent of the patients experienced Hgb
increases greater than 2 g/dL. Guidelines for the use of EPO in anemia
associated with hematologic and nonhematologic malignancy were pub-
95
94
96
THERAPY, COURSE, AND PROGNOSIS lished in 2002 and updated in 2007 and again in 2010. Because of
shared pathogenesis between anemia of cancer and AI, and the absence
Anemia that presents in the setting of infection, inflammation, or malig- of more specific recommendations, these form a reasonable guide for
nancy requires sufficient diagnostic studies to rule out reversible and the EPO treatment of AI. The guidelines (used and quoted or para-
potentially more threatening causes, such as occult hemorrhage; iron, phrased here with permission) recommend treating patients with Hgb
vitamin B , and folate deficiencies; hemolysis; and drug reaction. If the less than 10 g/dL when necessary to avoid red blood cell transfusions,
12
anemia can be designated as AI after such studies, effective treatment of and after discussion of the patient’s preferences between transfusion and
the underlying disease resolves the anemia. If treatment of the under- EPO treatment. Furthermore, the FDA recommends that dosing should
lying disease is not effective and the patient has symptoms or medical be “titrated for each patient to achieve and maintain the lowest hemo-
complications attributable to anemia, one or more of the available ane- globin level sufficient to avoid the need for blood transfusion.” Because
mia-specific treatment modalities should be considered (Table 37–3). of reports of increased risk of thromboembolism in patients receiving
These recommendations are also applicable to anemia of CKD where, these agents, clinicians should carefully weigh the risks of thromboem-
for most patients, only renal transplantation can reverse the underlying bolism in patients for whom ESAs are prescribed. An optimal target
pathology. However, although anemia generally resolves or improves Hgb concentration cannot be definitively determined from the available
after renal transplantation, 30 to 40 percent patients continue to be ane- literature. Modification to reduce the ESA dose is appropriate when Hgb
mic, mainly because of pathologic changes in the transplanted kidney reaches a level sufficient to avoid transfusion or the increase exceeds 1 g/
and adverse effects of immunosuppressive drugs. 71-78 dL in any 2-week period to avoid excessive ESA exposure. The FDA-ap-
Specific therapy for AI and anemia of CKD employs erythrocyte proved starting dose of epoetin is 150 U/kg three times a week or 40,000
transfusions, erythropoiesis-stimulating agents (ESAs) and intravenous U weekly subcutaneously. The FDA-approved starting dose of darbepo-
iron (see Table 37–3). Transfusion of erythrocytes is used to correct AI etin is 2.25 mcg/kg weekly or 500 mcg every 3 weeks subcutaneously.
or anemia of CKD when anemia is moderate to severe and the patient Alternative starting doses or dosing schedules have shown no consistent
is acutely symptomatic. Because treatment with ESAs often effectively difference in effectiveness on outcomes, including transfusion and Hgb
treats chronic anemia but may increase the risk of thromboembolic response, although they may be considered to improve convenience.
events, 79–82 guidelines have been proposed for appropriate use of these Dose escalation should follow FDA-approved labeling; no convincing
agents. The widespread adjunctive use of intravenous iron with ESAs evidence exists to suggest differences in dose escalation schedules are
may increase their effectiveness and reduce the required doses but associated with different effectiveness. Continuing the ESA treatment

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